Acute Heart fail Drugs (pt 2 HF cases) Flashcards
Dopamine actions
Stimulates release of catecholamines
Always hypothesized to be renal protective, but has never been shown to clinically significant.
Dosing of Dopamine changes it’s affects at
low doese of 2-5 mcg/kg/min:
doses greater then 6 mcg/kg/min:
doses of 10 mcg/kg/min:
Lower doses 2-5 mcg/kg/min exert effects on dopamine receptors and b receptors.
At doses greater than 6 mcg/kg/min:tachycardia without increased inotropypredominates.
at 10 mcg/kg/min: Afterload increases due to effects on a receptors
ACtion of Dobutamine:
Predominant action is a β1 agonist with weak β2 activity.
Increases contractility with mild vasodilator effect.
Predominant action is a β1 agonist with weak β2 activity.
Increases contractility with mild vasodilator effect.
Dobutamine
Side effect of Dobutamine
- ARRHYTHMIA
- ANGINA
- HYPERTENSION
- TACHYCARDIA
Levosimendan
Calcium sensitizer and Vasodilator
Acts on Troponin C to increase its sensitivity to calcium.
At high concentrations can be a phosphodiesterase III inhibitor
Acts on Troponin C to increase its sensitivity to calcium.
At high concentrations can be a phosphodiesterase III inhibitor
Levosimednan
Levosimendan effects on:
LVEDP:
Afterload:
SV:
Decrease LVEDP
Decrease Afterload
Increase Stroke Volume
What are the issues when using ionotropes in ADHF?
Arrythmias, hypotension, increased troponin release, increases in-hospital stay and 6 month mortality, doesn’t decrease hospital stay
What do we have to keep in mind when dosing diuretics in Heart fail pts?
dosing needs to be higher to achieve same effect we seen in non-HF pts.
What is the Braking phenomenon in regards to diuretic therapy?
“Braking” phenomenon
– Long-term loop diuretic administration results in a reduced natriuretic response
– Relative or absolute contraction of the extracellular fluid volume,
resulting in reduced delivery of solute to the proximal tubule via the RAAS and SNS as well as by enhanced distal nephron solute
reabsorption via adaptive epithelial hypertrophy and hyper function.
What is “rebound” phenomenon in regards to diuretics?
“Rebound”
– Infrequent dosing may lead to sodium retention that exceeds natriuresis.
– Divided doses to help with this, but hold off on it as long as possible
Why is long term tolerance an issue in Diuretic therapy in HF pts?
Long-term Tolerance
– Tubular hypertrophy to compensate for salt loss
Pt comes in with heart fail and your attending stays you will start them on diuretics, which one do you start them on?
Furosemide admin first; in IV as bolus or continous… if it’s refractory… switch to bumetadine
What type of electrolyte abnormalities do we see in diuretics?
HYPOKALEMIA
HYPOMAGNESEMIA
HYPONATREMIA
These drugs cause renal insufficiency when given with digoxin as well as gout exacerbation and cause muscle cramps if given too quickly.
Diuretics
You attending had you administered Bumetanide adn mirinone to pt in heart fail. Their saturation went up to 68% but the congestion isn’t improving… what do you do next?
re-eval (most likely have Na and fluid restriction)
Increase doses of loop diuretic or do continuous infusion. Additionally, add a second type of diuretic orally (metolazone or spironolactone)or IV chlorothaized
74 yo w/ longstanding history of poorly controlled HTN, DM and dyslipidemia; presents saturday AM with shortness of breath and wt gain; went to fish fry, didn’t take meds and took ibuprofen for back pain: medications include atenolol 25mg twice daily, HCTZ 25mg
daily, atorvastatin 20mg daily
BP 178/94 mm Hg, HR 90
• PE: Regular, crisp S1, S2, +S3, +S4
• JVP 8cm above clavicle
• Lungs clear with decreased BS at both bases
• 2+ LE edema
• Labs: Normal, except for NT-pro-BNP 4000
Dx?
Warm and Wet
increased JVD is sign of ‘wet’ as well as the LE edema (or any edema)
Not seeing signs of renal dysfunction or note of cool extremeties and labs aren’t showing renal dysnfunction so we think more warm as all those listed are signs of cool
Most pts wth acute decompensated HF fall into what category?
Wet and Warm
What are our key therapy goals in pts with wet and warm heart fail?
Decrease the filling pressures (LVEDP and PCWP)
Most of the time use IV diuretics and may need vasodialators
What vasodialators do we use in ADHF?
Nitroglycerin, nitroprusside, nesiritide
Effects of increasing doses of vasodialators: Afterload: Stroke Volume: LVEDP: Preload:
Afterload decreases
SV increases
LVEDP decreases
Preload decreases
IV nitroglycerin hemodynamic effects:
venodialator; arterial vasodilator at high doses
decreases filling pressure at low doses; at high doses, decreases SVR and increases cardiac output
Increased coronary blood flow
IV nitroglycerin has several major limitations; what are they?
headache, hypotension (especially if filling pressures are low), prolounged profound hypotension and bradycardia (rare), tachyphylaxsis and 20% don’t respond
